| First Author | Brand A | Year | 2020 |
| Journal | J Invest Dermatol | Volume | 140 |
| Issue | 1 | Pages | 132-142.e3 |
| PubMed ID | 31260672 | Mgi Jnum | J:285634 |
| Mgi Id | MGI:6387361 | Doi | 10.1016/j.jid.2019.06.132 |
| Citation | Brand A, et al. (2020) E-Cadherin is Dispensable to Maintain Langerhans Cells in the Epidermis. J Invest Dermatol 140(1):132-142.e3 |
| abstractText | The cell adhesion molecule E-cadherin is a major component of adherens junctions and marks Langerhans cells (LC), the only dendritic cell (DC) population of the epidermis. LC form a dense network and attach themselves to the surrounding keratinocytes via homophilic E-cadherin binding. LC activation, mobilization, and migration require a reduction in LC E-cadherin expression. To determine whether E-cadherin plays a role in regulating LC homeostasis and function, we generated CD11c-specific E-cadherin knockout mice (CD11c-Ecad(del)). In the absence of E-cadherin-mediated cell adhesion, LC numbers remained stable and similar as in control mice, even in aged animals. Intriguingly, E-cadherin-deficient LC displayed a dramatically changed morphology characterized by a more rounded cell body and fewer dendrites than wild-type cells. Nevertheless, maturation and migration of LC lacking E-cadherin was not altered, neither under steady-state nor inflammatory conditions. Accordingly, CD11c-Ecad(del) and control mice developed comparable contact hypersensitivity reactions and imiquimod-triggered psoriatic skin inflammation, indicating that E-cadherin on LC does not influence their ability to orchestrate T cell-mediated immunity. In conclusion, our data demonstrate that E-cadherin is dispensable to maintain LC in the epidermis and does not regulate LC maturation, migration, and function. |
